FAT ENERGY Flashcards

1
Q

sources of fat during exercise

A

intramscular triglycerides: primary source in high intensity
- trained individuals use muscle more effectively

plasma FFA: from adipose tissue lipolysis
- triglycerides –> FFA + glycerol
- low intensity
- important as musc glycogen lvls decline
- subcutaneous fat

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2
Q

lipolysis

A

breaking down of triglycerides via lipase enzymes

TGs are only useful fat for energy

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3
Q

how many carbons in FFAs

A

varies

this is why ATP produced via beta oxidation varies

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4
Q

main triglyceride sources

A
  1. adipocytes: fat storage across body via adipose tissue cells
  2. intramuscular TG
  3. blood lipoproteins: form of cholesterol i.e. HDL, LDL
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5
Q

6 stages of lipid breakdown

A
  1. mobilization
  2. transport
  3. uptake
  4. activation
  5. beta-oxidation
  6. mitochondrial oxidation
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6
Q

mobilization

A

triglyceride breakdown

hormone sensitive lipase: aka HSL
- ATP input needed for adipose and muscle activation

lipoprotein lipase: LPL

***ATP cleaves FFA off, which are then transported to muscle for energy
- 1 ATP/FFA
- remaining glycerol goes to liver to become glucose

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7
Q

transport

A

FFA circulates in blood by binding to ALBUMIN carrier protein
- bcs hydrophobic

in cells, FAs are activated via carnitine transferase…then transported across cell membrane into mitochondria for oxidation

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8
Q

uptake

A

active transport into muscle cytosol

special transport proteins used to move FFA

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9
Q

activation

A

prepare for breakdown

coa is added to FFA…becomes fatty acyl-coa
- this requires ATP

then moves across membrane into mitochondria via carrier

during b-oxidation, acyl coa is cleaved off

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10
Q

beta-oxidation

A

FFA is broken down in mitochondria

acyl coa dehydrogenase makes FAD –> FADH2

b-hydroxyacyl coa dehydrogenase makes NAD –> NADH

produces fatty acl coa, which is recycled to continue b-oxidation

also makes acetyl coa, which goes to krebs

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11
Q

mitochondrial oxidation

A

b-oxi products go to TCA and ETC

FADH2 and NADH go to ETC
acetyl coa goes to krebs

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12
Q

rule for b-oxi cycles and FAs

A

c/2 - 1 = number of cycles i.e. 7

of carbons is important i.e. 16c

of acetyl coa = #c/2 i.e. 8

b-oxi cannot occur with 2 carbons

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13
Q

products of b-oxi

A

each cycle makes:

1 NADH
1 FADH2
1 acetyl coa (3 NADH, 1 FADH, 1 ATP)

total 14 ATP
net = 12 ATP (2 invested to acquire FA)

2 invested PER fatty acid
- i.e. for 3 FAs, subtract 6 ATP

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14
Q

what does glycerol do after it’s cleaved from TG

A

can be used as energy source
- converted to form the liver can use for glycolysis
- does NOT contribute during exercise

1 ATP used to phosphorylate glycerol to G3P
- also reduces NAD –> NADH
- proceeds to glycolysis, making pyruvate

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15
Q

glycerol metabolism

A

glycerol –> G3P

2 ATP + 2 NADH + acetyl coa (3 nadh, 1 fadh, 1 atp)

1 glycerol = 17 ATP
net = 16

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16
Q

what about protein

A

contributes very little
has nitrogen, even more steps to become energy

not often used

17
Q

carb vs fat

A

carb: limited stores
fat: almost unlimited

carb 20% more efficient, allows exercise at high intensity
- faster rate, less o2 use

18
Q

when do energy systems contribute

A

phosphagen 10 seconds
anaerobic 1-2mins
equal by 75s
aerobic dominates after 2 minutes

19
Q

which system dominates at rest

A

aerobic, almost 100% ATP

20
Q

MET

A

metabolic equivalent of a task

1 MET = 3.5ml/kg/min
- resting o2 consumption

is relative to person’s musc mass

21
Q

vo2

A

volume of o2 consumed/minute

L/min is absolute value

ml/kg/min when divide by body weight…allows to compare size/BW effectively

the larger the person, the higher the absolute vo2

22
Q

rest-to-exercise transition

A

ATP production immediately increases

o2 uptake rapid inc, but NOT instantaneous

steady state w/in 1-4 mins after ATP requirement is met thru aerobic metabolism

23
Q

o2 deficit vs o2 debt

A

o2 deficit: lag in o2 uptake at beginning of exercise

o2 debt: repayment for o2 deficit at onset of exercise
- original term for EPOC

24
Q

recovery from exercise

A

o2 uptake remains elevated above rest

EPOC: excess post-exercise oxygen consumption
- repayment for o2 deficit
- separated by rapid and slow phase

25
Q

rapid vs slow phase EPOC

A

rapid phase: steep decline in vo2 (consumption) post-exercise
- 2-3mins
- o2 needed to resynthesize ATP and PCr, and replace tissue stores of o2
- 20% EPOC

slow phase: 30 minutes post exercise, slow dec in o2 consumption

why o2 is still elevated after exercise:
1. gluconeogenesis from lactate
2. HR and breathing elevated
3. elevated blood temp
4. elevated hormone concentration
5. others: glycogen depletion, ph restoration, uncoupling ATP

26
Q

comparing trained vs untrained EPOC and lactate

A

trained: lower o2 deficit, better developed aerobic capacity
- bcs of CV and musc adaptations
- less lactate and H production
- faster o2 uptake via offloading to muscles

27
Q

fate of lactate

A

used as fuel for heart and brain
- becomes acetyl-coa

oxidized in other tissues 60%

forms glucose in liver and stores as glycogen 25%

forms proteins 15%

excreted

28
Q

lactate shuttle

A

lactate is produced in one tissue and moves to another

bcs lactate is an important cell signal/fuel
- originally thought as waste

29
Q

how does lactate become glucose

A

by the cori cycle in the liver

30
Q

cori cycle

A

lactate produced by muscle and is transported to liver
- a lactate shuttle

in liver, lactate becomes glucose via gluconeogenesis

glucose transports to muscle, where it’s used in glycolysis

31
Q

lactate threshold

A

point where blood lactate concentration rises systematically during incremental exercise
- aka pt where lactate accumulates
- also called anaerobic threshold

when blood lactate lvls are 1mmol/L GREATER than resting values

no longer able to handle lactate production rate
- if continue, become fatigued

trained ppl reach threshold later, closer to VO2 max

32
Q

OBLA

A

onset of blood lactate accumulation

when blood lactate lvls reach 4mmol/L
- not above rest
- begins to accumulate at more accelerated rate

train to perform at this lvl for as long as possible

33
Q

what causes ppl to reach lactate threshold faster

A

low musc o2
accelerated glycolysis, produces more lactate
recruitment of fast twitch fibres: fatiguable
reduced lactate removal
LDH isozyme: catalyzes lactic acid + LDH –> lactate

34
Q

why do we measure lactate threshold

A
  1. training status
  2. predicts endurance performance
  3. establishes training intensity…program to inc threshold
35
Q

specificity of OBLA

A

characterized by exercise task specificity

diff exercise modes CANNOT have interchangeable OBLA

i.e. cannot compare running to cycling

36
Q

crossover concept

A

shift from fat to carb as intensity increases

due to recruitment of fast twitch fibres and inc blood levels of epinephrine